Dr Mujeeb Rehuman
drmujeebrehuman@rediffmail.com
Dementia is not a specific disease. It is a descriptive term
for a collection of symptoms that can be caused by a number of
disorders that affect the brain. People with dementia have
significantly impaired intellectual functioning that interferes with
normal activities and relationships. They also lose their ability to
solve problems and maintain emotional control, and they may
experience personality changes and behavioral problems such as
agitation, delusions, and hallucinations. While memory loss is a
common symptom of dementia, memory loss by itself does not mean that
a person has dementia. Doctors diagnose dementia only if two or more
brain functions - such as memory, language skills, perception, or
cognitive skills including reasoning and judgment - are significantly
impaired without loss of consciousness.
for a collection of symptoms that can be caused by a number of
disorders that affect the brain. People with dementia have
significantly impaired intellectual functioning that interferes with
normal activities and relationships. They also lose their ability to
solve problems and maintain emotional control, and they may
experience personality changes and behavioral problems such as
agitation, delusions, and hallucinations. While memory loss is a
common symptom of dementia, memory loss by itself does not mean that
a person has dementia. Doctors diagnose dementia only if two or more
brain functions - such as memory, language skills, perception, or
cognitive skills including reasoning and judgment - are significantly
impaired without loss of consciousness.
There are many disorders that can cause dementia. Some, such as AD,
lead to a progressive loss of mental functions. But other types of
dementia can be halted or reversed with appropriate treatment.
lead to a progressive loss of mental functions. But other types of
dementia can be halted or reversed with appropriate treatment.
With AD and many other types of dementia, disease processes cause
many nerve cells to stop functioning, lose connections with other
neurons, and die. In contrast, normal aging does not result in the
loss of large numbers of neurons in the brain.
many nerve cells to stop functioning, lose connections with other
neurons, and die. In contrast, normal aging does not result in the
loss of large numbers of neurons in the brain.
Different
Kinds of Dementia
Kinds of Dementia
Dementing disorders can be classified many different ways. These
classification schemes attempt to group disorders that have
particular features in common, such as whether they are progressive
or what parts of the brain are affected. Some frequently used
classifications include the following:
classification schemes attempt to group disorders that have
particular features in common, such as whether they are progressive
or what parts of the brain are affected. Some frequently used
classifications include the following:
Cortical
dementia: dementia where the brain damage primarily affects the
brain's cortex, or outer layer. Cortical dementias tend to cause
problems with memory, language, thinking, and social behavior.
Subcortical
dementia: dementia that affects parts of the brain below the
cortex. Subcortical dementia tends to cause changes in emotions and
movement in addition to problems with memory.
Progressive
dementia: dementia that gets worse over time, gradually
interfering with more and more cognitive abilities.
Primary dementia:
dementia such as AD that does not result from any other disease.
Secondary
dementia: dementia that occurs as a result of a physical disease
or injury.
Some types of dementia fit into more than one of these
classifications. For example, AD is considered both a progressive and
a cortical dementia.
classifications. For example, AD is considered both a progressive and
a cortical dementia.
Alzheimer's
disease
disease
Alzheimer's disease is the most common cause of dementia in people
aged 65 and older. In most people, symptoms of AD appear after age
60. However, there are some early-onset forms of the disease, usually
linked to a specific gene defect, which may appear as early as age
30. AD usually causes a gradual decline in cognitive abilities,
usually during a span of 7 to 10 years. Nearly all brain functions,
including memory, movement, language, judgment, behavior, and
abstract thinking, are eventually affected.
aged 65 and older. In most people, symptoms of AD appear after age
60. However, there are some early-onset forms of the disease, usually
linked to a specific gene defect, which may appear as early as age
30. AD usually causes a gradual decline in cognitive abilities,
usually during a span of 7 to 10 years. Nearly all brain functions,
including memory, movement, language, judgment, behavior, and
abstract thinking, are eventually affected.
AD is characterized by two abnormalities in the brain: amyloid
plaques and neurofibrillary tangles. Amyloid plaques,
which are found in the tissue between the nerve cells, are unusual
clumps of a protein called beta amyloid along with degenerating bits
of neurons and other cells.
plaques and neurofibrillary tangles. Amyloid plaques,
which are found in the tissue between the nerve cells, are unusual
clumps of a protein called beta amyloid along with degenerating bits
of neurons and other cells.
Neurofibrillary tangles are bundles of twisted filaments found within
neurons. These tangles are largely made up of a protein called tau.
In healthy neurons, the tau protein helps the functioning of
microtubules, which are part of the cell's structural support and
deliver substances throughout the nerve cell. However, in AD, tau is
changed in a way that causes it to twist into pairs of helical
filaments that collect into tangles. When this happens, the
microtubules cannot function correctly and they disintegrate. This
collapse of the neuron's transport system may impair communication
between nerve cells and cause them to die.
neurons. These tangles are largely made up of a protein called tau.
In healthy neurons, the tau protein helps the functioning of
microtubules, which are part of the cell's structural support and
deliver substances throughout the nerve cell. However, in AD, tau is
changed in a way that causes it to twist into pairs of helical
filaments that collect into tangles. When this happens, the
microtubules cannot function correctly and they disintegrate. This
collapse of the neuron's transport system may impair communication
between nerve cells and cause them to die.
Researchers do not know if amyloid plaques and neurofibrillary
tangles are harmful or if they are merely side effects of the disease
process that damages neurons and leads to the symptoms of AD. They do
know that plaques and tangles usually increase in the brain as AD
progresses.
tangles are harmful or if they are merely side effects of the disease
process that damages neurons and leads to the symptoms of AD. They do
know that plaques and tangles usually increase in the brain as AD
progresses.
In the early stages of AD, patients may experience memory impairment,
lapses of judgment, and subtle changes in personality. As the
disorder progresses, memory and language problems worsen and patients
begin to have difficulty performing activities of daily living, such
as balancing a checkbook or remembering to take medications. They
also may have visuospatial problems, such as difficulty navigating an
unfamiliar route. They may become disoriented about places and times,
may suffer delusions (such as the idea that someone is stealing from
them or that their spouse is being unfaithful), and may become
short-tempered and hostile. During the late stages of the disease,
patients begin to lose the ability to control motor functions. They
may have difficulty swallowing and lose bowel and bladder control.
They eventually lose the ability to recognize family members and to
speak. As AD progresses, it begins to affect the person's emotions
and behavior. Most people with AD eventually develop symptoms such as
aggression, agitation, depression, sleeplessness, or delusions.
lapses of judgment, and subtle changes in personality. As the
disorder progresses, memory and language problems worsen and patients
begin to have difficulty performing activities of daily living, such
as balancing a checkbook or remembering to take medications. They
also may have visuospatial problems, such as difficulty navigating an
unfamiliar route. They may become disoriented about places and times,
may suffer delusions (such as the idea that someone is stealing from
them or that their spouse is being unfaithful), and may become
short-tempered and hostile. During the late stages of the disease,
patients begin to lose the ability to control motor functions. They
may have difficulty swallowing and lose bowel and bladder control.
They eventually lose the ability to recognize family members and to
speak. As AD progresses, it begins to affect the person's emotions
and behavior. Most people with AD eventually develop symptoms such as
aggression, agitation, depression, sleeplessness, or delusions.
On average, patients with AD live for 8 to 10 years after they are
diagnosed. However, some people live as long as 20 years. Patients
with AD often die of aspiration pneumonia because they lose the
ability to swallow late in the course of the disease.
diagnosed. However, some people live as long as 20 years. Patients
with AD often die of aspiration pneumonia because they lose the
ability to swallow late in the course of the disease.
Vascular
dementia
dementia
Vascular dementia is the second most common cause of dementia, after
AD. It accounts for up to 20 percent of all dementias and is caused
by brain damage from cerebrovascular or cardiovascular problems -
usually strokes. It also may result from genetic diseases,
endocarditis (infection of a heart valve), or amyloid angiopathy (a
process in which amyloid protein builds up in the brain's blood
vessels, sometimes causing hemorrhagic or "bleeding"
strokes). In many cases, it may coexist with AD. The incidence of
vascular dementia increases with advancing age and is similar in men
and women.
AD. It accounts for up to 20 percent of all dementias and is caused
by brain damage from cerebrovascular or cardiovascular problems -
usually strokes. It also may result from genetic diseases,
endocarditis (infection of a heart valve), or amyloid angiopathy (a
process in which amyloid protein builds up in the brain's blood
vessels, sometimes causing hemorrhagic or "bleeding"
strokes). In many cases, it may coexist with AD. The incidence of
vascular dementia increases with advancing age and is similar in men
and women.
Symptoms of vascular dementia often begin suddenly, frequently after
a stroke. Patients may have a history of high blood pressure,
vascular disease, or previous strokes or heart attacks. Vascular
dementia may or may not get worse with time, depending on whether the
person has additional strokes. In some cases, symptoms may get better
with time. When the disease does get worse, it often progresses in a
stepwise manner, with sudden changes in ability. Vascular dementia
with brain damage to the mid-brain regions, however, may cause a
gradual, progressive cognitive impairment that may look much like AD.
Unlike people with AD, people with vascular dementia often maintain
their personality and normal levels of emotional responsiveness until
the later stages of the disease.
a stroke. Patients may have a history of high blood pressure,
vascular disease, or previous strokes or heart attacks. Vascular
dementia may or may not get worse with time, depending on whether the
person has additional strokes. In some cases, symptoms may get better
with time. When the disease does get worse, it often progresses in a
stepwise manner, with sudden changes in ability. Vascular dementia
with brain damage to the mid-brain regions, however, may cause a
gradual, progressive cognitive impairment that may look much like AD.
Unlike people with AD, people with vascular dementia often maintain
their personality and normal levels of emotional responsiveness until
the later stages of the disease.
People with vascular dementia frequently wander at night and often
have other problems commonly found in people who have had a stroke,
including depression and incontinence.
have other problems commonly found in people who have had a stroke,
including depression and incontinence.
There are several types of vascular dementia, which vary slightly in
their causes and symptoms. One type, called multi-infarct dementia
(MID), is caused by numerous small strokes in the brain. MID
typically includes multiple damaged areas, called infarcts, along
with extensive lesions in the white matter, or nerve fibers, of the
brain.
their causes and symptoms. One type, called multi-infarct dementia
(MID), is caused by numerous small strokes in the brain. MID
typically includes multiple damaged areas, called infarcts, along
with extensive lesions in the white matter, or nerve fibers, of the
brain.
Because the infarcts in MID affect isolated areas of the brain, the
symptoms are often limited to one side of the body or they may affect
just one or a few specific functions, such as language. Neurologists
call these "local" or "focal" symptoms, as
opposed to the "global" symptoms seen in AD, which affect
many functions and are not restricted to one side of the body.
symptoms are often limited to one side of the body or they may affect
just one or a few specific functions, such as language. Neurologists
call these "local" or "focal" symptoms, as
opposed to the "global" symptoms seen in AD, which affect
many functions and are not restricted to one side of the body.
Although not all strokes cause dementia, in some cases a single
stroke can damage the brain enough to cause dementia. This condition
is called single-infarct dementia. Dementia is more common when the
stroke takes place on the left side (hemisphere) of the brain and/or
when it involves the hippocampus, a brain structure important for
memory.
stroke can damage the brain enough to cause dementia. This condition
is called single-infarct dementia. Dementia is more common when the
stroke takes place on the left side (hemisphere) of the brain and/or
when it involves the hippocampus, a brain structure important for
memory.
Another type of vascular dementia is called Binswanger's disease.
This rare form of dementia is characterized by damage to small blood
vessels in the white matter of the brain (white matter is found in
the inner layers of the brain and contains many nerve fibers coated
with a whitish, fatty substance called myelin). Binswanger's disease
leads to brain lesions, loss of memory, disordered cognition, and
mood changes. Patients with this disease often show signs of abnormal
blood pressure, stroke, blood abnormalities, disease of the large
blood vessels in the neck, and/or disease of the heart valves. Other
prominent features include urinary incontinence, difficulty walking,
clumsiness, slowness, lack of facial expression, and speech
difficulty. These symptoms, which usually begin after the age of 60,
are not always present in all patients and may sometimes appear only
temporarily. Treatment of Binswanger's disease is symptomatic, and
may include the use of medications to control high blood pressure,
depression, heart arrhythmias, and low blood pressure. The disorder
often includes episodes of partial recovery.
This rare form of dementia is characterized by damage to small blood
vessels in the white matter of the brain (white matter is found in
the inner layers of the brain and contains many nerve fibers coated
with a whitish, fatty substance called myelin). Binswanger's disease
leads to brain lesions, loss of memory, disordered cognition, and
mood changes. Patients with this disease often show signs of abnormal
blood pressure, stroke, blood abnormalities, disease of the large
blood vessels in the neck, and/or disease of the heart valves. Other
prominent features include urinary incontinence, difficulty walking,
clumsiness, slowness, lack of facial expression, and speech
difficulty. These symptoms, which usually begin after the age of 60,
are not always present in all patients and may sometimes appear only
temporarily. Treatment of Binswanger's disease is symptomatic, and
may include the use of medications to control high blood pressure,
depression, heart arrhythmias, and low blood pressure. The disorder
often includes episodes of partial recovery.
Another type of vascular dementia is linked to a rare hereditary
disorder called CADASIL, which stands for cerebral
autosomal dominant arteriopathy with subcortical infarct and
leukoencephalopathy. CADASIL is linked to abnormalities of a
specific gene, Notch3, which is located on chromosome 19. This
condition causes multi-infarct dementia as well as stroke, migraine
with aura, and mood disorders. The first symptoms usually appear in
people who are in their twenties, thirties, or forties and affected
individuals often die by age 65. Researchers believe most people with
CADASIL go undiagnosed, and the actual prevalence of the disease is
not yet known.
disorder called CADASIL, which stands for cerebral
autosomal dominant arteriopathy with subcortical infarct and
leukoencephalopathy. CADASIL is linked to abnormalities of a
specific gene, Notch3, which is located on chromosome 19. This
condition causes multi-infarct dementia as well as stroke, migraine
with aura, and mood disorders. The first symptoms usually appear in
people who are in their twenties, thirties, or forties and affected
individuals often die by age 65. Researchers believe most people with
CADASIL go undiagnosed, and the actual prevalence of the disease is
not yet known.
Other causes of vascular dementia include vasculitis, an
inflammation of the blood vessel system; profound hypotension (low
blood pressure); and lesions caused by brain hemorrhage. The
autoimmune disease lupus erythematosus and the inflammatory disease
temporal arteritis can also damage blood vessels in a way that leads
to vascular dementia.
inflammation of the blood vessel system; profound hypotension (low
blood pressure); and lesions caused by brain hemorrhage. The
autoimmune disease lupus erythematosus and the inflammatory disease
temporal arteritis can also damage blood vessels in a way that leads
to vascular dementia.
Lewy
body dementia (LBD)
body dementia (LBD)
Lewy body
dementia (LBD) is one of the most common types of progressive
dementia. LBD usually occurs sporadically, in people with no known
family history of the disease. However, rare familial cases have
occasionally been reported.
dementia (LBD) is one of the most common types of progressive
dementia. LBD usually occurs sporadically, in people with no known
family history of the disease. However, rare familial cases have
occasionally been reported.
In LBD, cells die in the brain's cortex, or outer layer, and in a
part of the mid-brain called the substantia nigra. Many of the
remaining nerve cells in the substantia nigra contain abnormal
structures called Lewy bodies that are the hallmark of the disease.
Lewy bodies may also appear in the brain's cortex, or outer layer.
Lewy bodies contain a protein called alpha-synuclein that has been
linked to Parkinson's disease and several other disorders.
Researchers, who sometimes refer to these disorders collectively as
"synucleinopathies," do not yet know why this protein
accumulates inside nerve cells in LBD.
part of the mid-brain called the substantia nigra. Many of the
remaining nerve cells in the substantia nigra contain abnormal
structures called Lewy bodies that are the hallmark of the disease.
Lewy bodies may also appear in the brain's cortex, or outer layer.
Lewy bodies contain a protein called alpha-synuclein that has been
linked to Parkinson's disease and several other disorders.
Researchers, who sometimes refer to these disorders collectively as
"synucleinopathies," do not yet know why this protein
accumulates inside nerve cells in LBD.
The symptoms of LBD overlap with AD in many ways, and may include
memory impairment, poor judgment, and confusion. However, LBD
typically also includes visual hallucinations, parkinsonian symptoms
such as a shuffling gait and flexed posture, and day-to-day
fluctuations in the severity of symptoms. Patients with LBD live an
average of 7 years after symptoms begin.
memory impairment, poor judgment, and confusion. However, LBD
typically also includes visual hallucinations, parkinsonian symptoms
such as a shuffling gait and flexed posture, and day-to-day
fluctuations in the severity of symptoms. Patients with LBD live an
average of 7 years after symptoms begin.
There is no cure for LBD, and treatments are aimed at controlling the
parkinsonian and psychiatric symptoms of the disorder. Patients
sometimes respond dramatically to treatment with antiparkinsonian
drugs and/or cholinesterase inhibitors, such as those used for AD.
Some studies indicate that neuroleptic drugs, such as clozapine and
olanzapine, also can reduce the psychiatric symptoms of this disease.
But neuroleptic drugs may cause severe adverse reactions, so other
therapies should be tried first and patients using these drugs should
be closely monitored.
parkinsonian and psychiatric symptoms of the disorder. Patients
sometimes respond dramatically to treatment with antiparkinsonian
drugs and/or cholinesterase inhibitors, such as those used for AD.
Some studies indicate that neuroleptic drugs, such as clozapine and
olanzapine, also can reduce the psychiatric symptoms of this disease.
But neuroleptic drugs may cause severe adverse reactions, so other
therapies should be tried first and patients using these drugs should
be closely monitored.
Lewy bodies are often found in the brains of people with Parkinson's
and AD. These findings suggest that either LBD is related to these
other causes of dementia or that the diseases sometimes coexist in
the same person.
and AD. These findings suggest that either LBD is related to these
other causes of dementia or that the diseases sometimes coexist in
the same person.
Frontotemporal
dementia (FTD)
dementia (FTD)
Frontotemporal dementia (FTD), sometimes called frontal lobe
dementia, describes a group of diseases characterized by degeneration
of nerve cells - especially those in the frontal and temporal lobes
of the brain. Unlike AD, FTD usually does not include formation of
amyloid plaques. In many people with FTD, there is an abnormal form
of tau protein in the brain, which accumulates into neurofibrillary
tangles. This disrupts normal cell activities and may cause the cells
to die.
dementia, describes a group of diseases characterized by degeneration
of nerve cells - especially those in the frontal and temporal lobes
of the brain. Unlike AD, FTD usually does not include formation of
amyloid plaques. In many people with FTD, there is an abnormal form
of tau protein in the brain, which accumulates into neurofibrillary
tangles. This disrupts normal cell activities and may cause the cells
to die.
Experts believe FTD accounts for 2 to 10 percent of all cases of
dementia. Symptoms of FTD usually appear between the ages of 40 and
65. In many cases, people with FTD have a family history of dementia,
suggesting that there is a strong genetic factor in the disease. The
duration of FTD varies, with some patients declining rapidly over 2
to 3 years and others showing only minimal changes for many years.
People with FTD live with the disease for an average of 5 to 10 years
after diagnosis.
dementia. Symptoms of FTD usually appear between the ages of 40 and
65. In many cases, people with FTD have a family history of dementia,
suggesting that there is a strong genetic factor in the disease. The
duration of FTD varies, with some patients declining rapidly over 2
to 3 years and others showing only minimal changes for many years.
People with FTD live with the disease for an average of 5 to 10 years
after diagnosis.
Because structures found in the frontal and temporal lobes of the
brain control judgment and social behavior, people with FTD often
have problems maintaining normal interactions and following social
conventions. They may steal or exhibit impolite and socially
inappropriate behavior, and they may neglect their normal
responsibilities. Other common symptoms include loss of speech and
language, compulsive or repetitive behavior, increased appetite, and
motor problems such as stiffness and balance problems. Memory loss
also may occur, although it typically appears late in the disease.
brain control judgment and social behavior, people with FTD often
have problems maintaining normal interactions and following social
conventions. They may steal or exhibit impolite and socially
inappropriate behavior, and they may neglect their normal
responsibilities. Other common symptoms include loss of speech and
language, compulsive or repetitive behavior, increased appetite, and
motor problems such as stiffness and balance problems. Memory loss
also may occur, although it typically appears late in the disease.
In one type of FTD called Pick's disease, certain nerve cells become
abnormal and swollen before they die. These swollen, or ballooned,
neurons are one hallmark of the disease. The brains of people with
Pick's disease also have abnormal structures called Pick bodies,
composed largely of the protein tau, inside the neurons. The cause of
Pick's disease is unknown, but it runs in some families and thus it
is probably due at least in part to a faulty gene or genes. The
disease usually begins after age 50 and causes changes in personality
and behavior that gradually worsen over time. The symptoms of Pick's
disease are very similar to those of AD, and may include
inappropriate social behavior, loss of mental flexibility, language
problems, and difficulty with thinking and concentration. There is
currently no way to slow the progressive degeneration found in Pick's
disease. However, medication may be helpful in reducing aggression
and other behavioral problems, and in treating depression.
abnormal and swollen before they die. These swollen, or ballooned,
neurons are one hallmark of the disease. The brains of people with
Pick's disease also have abnormal structures called Pick bodies,
composed largely of the protein tau, inside the neurons. The cause of
Pick's disease is unknown, but it runs in some families and thus it
is probably due at least in part to a faulty gene or genes. The
disease usually begins after age 50 and causes changes in personality
and behavior that gradually worsen over time. The symptoms of Pick's
disease are very similar to those of AD, and may include
inappropriate social behavior, loss of mental flexibility, language
problems, and difficulty with thinking and concentration. There is
currently no way to slow the progressive degeneration found in Pick's
disease. However, medication may be helpful in reducing aggression
and other behavioral problems, and in treating depression.
In some cases, familial FTD is linked to a mutation in the tau gene.
This disorder, called frontotemporal dementia with parkinsonism
linked to chromosome 17 (FTDP-17), is much like other types of FTD
but often includes psychiatric symptoms such as delusions and
hallucinations.
This disorder, called frontotemporal dementia with parkinsonism
linked to chromosome 17 (FTDP-17), is much like other types of FTD
but often includes psychiatric symptoms such as delusions and
hallucinations.
Primary progressive aphasia (PPA) is a type of FTD that may begin in
people as early as their forties. "Aphasia" is a general
term used to refer to deficits in language functions, such as
speaking, understanding what others are saying, and naming common
objects. In PPA one or more of these functions can become impaired.
Symptoms often begin gradually and progress slowly over a period of
years. As the disease progresses, memory and attention may also be
impaired and patients may show personality and behavior changes.
Many, but not all, people with PPA eventually develop symptoms of
dementia.
people as early as their forties. "Aphasia" is a general
term used to refer to deficits in language functions, such as
speaking, understanding what others are saying, and naming common
objects. In PPA one or more of these functions can become impaired.
Symptoms often begin gradually and progress slowly over a period of
years. As the disease progresses, memory and attention may also be
impaired and patients may show personality and behavior changes.
Many, but not all, people with PPA eventually develop symptoms of
dementia.
HIV-associated
dementia (HAD)
dementia (HAD)
HIV-associated dementia (HAD) results from infection with the human
immunodeficiency virus (HIV) that causes AIDS. HAD can cause
widespread destruction of the brain's white matter. This leads to a
type of dementia that generally includes impaired memory, apathy,
social withdrawal, and difficulty concentrating. People with HAD
often develop movement problems as well. There is no specific
treatment for HAD, but AIDS drugs can delay onset of the disease and
may help to reduce symptoms.
immunodeficiency virus (HIV) that causes AIDS. HAD can cause
widespread destruction of the brain's white matter. This leads to a
type of dementia that generally includes impaired memory, apathy,
social withdrawal, and difficulty concentrating. People with HAD
often develop movement problems as well. There is no specific
treatment for HAD, but AIDS drugs can delay onset of the disease and
may help to reduce symptoms.
Huntington's
disease (HD)
disease (HD)
Huntington's disease (HD) is a hereditary disorder caused by a faulty
gene for a protein called huntingtin. The children of people with the
disorder have a 50 percent chance of inheriting it. The disease
causes degeneration in many regions of the brain and spinal cord.
Symptoms of HD usually begin when patients are in their thirties or
forties, and the average life expectancy after diagnosis is about 15
years.
gene for a protein called huntingtin. The children of people with the
disorder have a 50 percent chance of inheriting it. The disease
causes degeneration in many regions of the brain and spinal cord.
Symptoms of HD usually begin when patients are in their thirties or
forties, and the average life expectancy after diagnosis is about 15
years.
Cognitive symptoms of HD typically begin with mild personality
changes, such as irritability, anxiety, and depression, and progress
to severe dementia. Many patients also show psychotic behavior. HD
causes chorea - involuntary jerky, arrhythmic movements of the body -
as well as muscle weakness, clumsiness, and gait disturbances.
changes, such as irritability, anxiety, and depression, and progress
to severe dementia. Many patients also show psychotic behavior. HD
causes chorea - involuntary jerky, arrhythmic movements of the body -
as well as muscle weakness, clumsiness, and gait disturbances.
Dementia
pugilistica
pugilistica
Dementia pugilistica, also called chronic traumatic encephalopathy or
Boxer's syndrome, is caused by head trauma, such as that experienced
by people who have been punched many times in the head during boxing.
The most common symptoms of the condition are dementia and
parkinsonism, which can appear many years after the trauma ends.
Affected individuals may also develop poor coordination and slurred
speech. A single traumatic brain injury may also lead to a disorder
called post-traumatic dementia (PTD). PTD is much like dementia
pugilistica but usually also includes long-term memory problems.
Other symptoms vary depending on which part of the brain was damaged
by the injury.
Boxer's syndrome, is caused by head trauma, such as that experienced
by people who have been punched many times in the head during boxing.
The most common symptoms of the condition are dementia and
parkinsonism, which can appear many years after the trauma ends.
Affected individuals may also develop poor coordination and slurred
speech. A single traumatic brain injury may also lead to a disorder
called post-traumatic dementia (PTD). PTD is much like dementia
pugilistica but usually also includes long-term memory problems.
Other symptoms vary depending on which part of the brain was damaged
by the injury.
Corticobasal
degeneration (CBD)
degeneration (CBD)
Corticobasal degeneration (CBD) is a progressive disorder
characterized by nerve cell loss and atrophy of multiple areas of the
brain. Brain cells from people with CBD often have abnormal
accumulations of the protein tau. CBD usually progresses gradually
over the course of 6 to 8 years. Initial symptoms, which typically
begin at or around age 60, may first appear on one side of the body
but eventually will affect both sides. Some of the symptoms, such as
poor coordination and rigidity, are similar to those found in
Parkinson's disease. Other symptoms may include memory loss,
dementia, visual-spatial problems, apraxia (loss of the ability to
make familiar, purposeful movements), hesitant and halting speech,
myoclonus (involuntary muscular jerks), and dysphagia (difficulty
swallowing). Death is often caused by pneumonia or other secondary
problems such as sepsis (severe infection of the blood) or pulmonary
embolism (a blood clot in the lungs).
characterized by nerve cell loss and atrophy of multiple areas of the
brain. Brain cells from people with CBD often have abnormal
accumulations of the protein tau. CBD usually progresses gradually
over the course of 6 to 8 years. Initial symptoms, which typically
begin at or around age 60, may first appear on one side of the body
but eventually will affect both sides. Some of the symptoms, such as
poor coordination and rigidity, are similar to those found in
Parkinson's disease. Other symptoms may include memory loss,
dementia, visual-spatial problems, apraxia (loss of the ability to
make familiar, purposeful movements), hesitant and halting speech,
myoclonus (involuntary muscular jerks), and dysphagia (difficulty
swallowing). Death is often caused by pneumonia or other secondary
problems such as sepsis (severe infection of the blood) or pulmonary
embolism (a blood clot in the lungs).
There are no specific treatments available for CBD. Drugs such as
clonazepam may help with myoclonus, however, and occupational,
physical, and speech therapy can help in managing the disabilities
associated with this disease. The symptoms of the disease often do
not respond to Parkinson's medications or other drugs.
clonazepam may help with myoclonus, however, and occupational,
physical, and speech therapy can help in managing the disabilities
associated with this disease. The symptoms of the disease often do
not respond to Parkinson's medications or other drugs.
Creutzfeldt-Jakob
disease (CJD)
disease (CJD)
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, fatal brain
disorder that affects about one in every million people per year
worldwide. Symptoms usually begin after age 60 and most patients die
within 1 year. Many researchers believe CJD results from an abnormal
form of a protein called a prion. Most cases of CJD occur
sporadically - that is, in people who have no known risk factors for
the disease. However, about 5 to 10 percent of cases of CJD in the
United States are hereditary, caused by a mutation in the gene for
the prion protein. In rare cases, CJD can also be acquired through
exposure to diseased brain or nervous system tissue, usually through
certain medical procedures. There is no evidence that CJD is
contagious through the air or through casual contact with a CJD
patient.
disorder that affects about one in every million people per year
worldwide. Symptoms usually begin after age 60 and most patients die
within 1 year. Many researchers believe CJD results from an abnormal
form of a protein called a prion. Most cases of CJD occur
sporadically - that is, in people who have no known risk factors for
the disease. However, about 5 to 10 percent of cases of CJD in the
United States are hereditary, caused by a mutation in the gene for
the prion protein. In rare cases, CJD can also be acquired through
exposure to diseased brain or nervous system tissue, usually through
certain medical procedures. There is no evidence that CJD is
contagious through the air or through casual contact with a CJD
patient.
Patients with CJD may initially experience problems with muscular
coordination; personality changes, including impaired memory,
judgment, and thinking; and impaired vision. Other symptoms may
include insomnia and depression. As the illness progresses, mental
impairment becomes severe. Patients often develop myoclonus and they
may go blind. They eventually lose the ability to move and speak, and
go into a coma. Pneumonia and other infections often occur in these
patients and can lead to death.
coordination; personality changes, including impaired memory,
judgment, and thinking; and impaired vision. Other symptoms may
include insomnia and depression. As the illness progresses, mental
impairment becomes severe. Patients often develop myoclonus and they
may go blind. They eventually lose the ability to move and speak, and
go into a coma. Pneumonia and other infections often occur in these
patients and can lead to death.
CJD belongs to a family of human and animal diseases known as the
transmissible spongiform encephalopathies (TSEs). Spongiform refers
to the characteristic appearance of infected brains, which become
filled with holes until they resemble sponges when viewed under a
microscope. CJD is the most common of the known human TSEs. Others
include fatal familial insomnia and Gerstmann-Straussler-Scheinker
disease (see below).
transmissible spongiform encephalopathies (TSEs). Spongiform refers
to the characteristic appearance of infected brains, which become
filled with holes until they resemble sponges when viewed under a
microscope. CJD is the most common of the known human TSEs. Others
include fatal familial insomnia and Gerstmann-Straussler-Scheinker
disease (see below).
In recent years, a new type of CJD, called variant CJD (vCJD), has
been found in Great Britain and several other European countries. The
initial symptoms of vCJD are different from those of classic CJD and
the disorder typically occurs in younger patients. Research suggests
that vCJD may have resulted from human consumption of beef from
cattle with a TSE disease called bovine spongiform encephalopathy
(BSE), also known as "mad cow disease."
been found in Great Britain and several other European countries. The
initial symptoms of vCJD are different from those of classic CJD and
the disorder typically occurs in younger patients. Research suggests
that vCJD may have resulted from human consumption of beef from
cattle with a TSE disease called bovine spongiform encephalopathy
(BSE), also known as "mad cow disease."
Other
rare hereditary dementias
rare hereditary dementias
Other rare hereditary dementias include
Gerstmann-Straussler-Scheinker (GSS) disease, fatal familial
insomnia, familial British dementia, and familial Danish dementia.
Symptoms of GSS typically include ataxia and progressive dementia
that begins when people are between 50 and 60 years old. The disease
may last for several years before patients eventually die. Fatal
familial insomnia causes degeneration of a brain region called the
thalamus, which is partially responsible for controlling sleep. It
causes a progressive insomnia that eventually leads to a complete
inability to sleep. Other symptoms may include poor reflexes,
dementia, hallucinations, and eventually coma. It can be fatal within
7 to 13 months after symptoms begin but may last longer. Familial
British dementia and familial Danish dementia have been linked to two
different defects in a gene found on chromosome 13. The symptoms of
both diseases include progressive dementia, paralysis, and loss of
balance.
Gerstmann-Straussler-Scheinker (GSS) disease, fatal familial
insomnia, familial British dementia, and familial Danish dementia.
Symptoms of GSS typically include ataxia and progressive dementia
that begins when people are between 50 and 60 years old. The disease
may last for several years before patients eventually die. Fatal
familial insomnia causes degeneration of a brain region called the
thalamus, which is partially responsible for controlling sleep. It
causes a progressive insomnia that eventually leads to a complete
inability to sleep. Other symptoms may include poor reflexes,
dementia, hallucinations, and eventually coma. It can be fatal within
7 to 13 months after symptoms begin but may last longer. Familial
British dementia and familial Danish dementia have been linked to two
different defects in a gene found on chromosome 13. The symptoms of
both diseases include progressive dementia, paralysis, and loss of
balance.
Secondary
Dementias
Dementias
Dementia may occur in patients who have other disorders that
primarily affect movement or other functions. These cases are often
referred to as secondary dementias. The relationship between these
disorders and the primary dementias is not always clear. For
instance, people with advanced Parkinson's disease, which is
primarily a movement disorder, sometimes develop symptoms of
dementia. Many Parkinson's patients also have amyloid plaques and
neurofibrillary tangles like those found in AD. The two diseases may
be linked in a yet-unknown way, or they may simply coexist in some
people. People with Parkinson's and associated dementia sometimes
show signs of Lewy body dementia or progressive supranuclear palsy at
autopsy, suggesting that these diseases may also overlap with
Parkinson's or that Parkinson's is sometimes misdiagnosed.
primarily affect movement or other functions. These cases are often
referred to as secondary dementias. The relationship between these
disorders and the primary dementias is not always clear. For
instance, people with advanced Parkinson's disease, which is
primarily a movement disorder, sometimes develop symptoms of
dementia. Many Parkinson's patients also have amyloid plaques and
neurofibrillary tangles like those found in AD. The two diseases may
be linked in a yet-unknown way, or they may simply coexist in some
people. People with Parkinson's and associated dementia sometimes
show signs of Lewy body dementia or progressive supranuclear palsy at
autopsy, suggesting that these diseases may also overlap with
Parkinson's or that Parkinson's is sometimes misdiagnosed.
Other disorders that may include symptoms of dementia include
multiple sclerosis; presenile dementia with motor neuron disease,
also called ALS dementia; olivopontocerebellar atrophy (OPCA);
Wilson's disease; and normal pressure hydrocephalus (NPH).
multiple sclerosis; presenile dementia with motor neuron disease,
also called ALS dementia; olivopontocerebellar atrophy (OPCA);
Wilson's disease; and normal pressure hydrocephalus (NPH).
Dementias
in Children
in Children
While it is usually found in adults, dementia can also occur in
children. For example, infections and poisoning can lead to dementia
in people of any age. In addition, some disorders unique to children
can cause dementia.
children. For example, infections and poisoning can lead to dementia
in people of any age. In addition, some disorders unique to children
can cause dementia.
Niemann-Pick
disease is a group of inherited disorders that affect metabolism
and are caused by specific genetic mutations. Patients with
Niemann-Pick disease cannot properly metabolize cholesterol and other
lipids. Consequently, excessive amounts of cholesterol accumulate in
the liver and spleen and excessive amounts of other lipids accumulate
in the brain. Symptoms may include dementia, confusion, and problems
with learning and memory. These diseases usually begin in young
school-age children but may also appear during the teen years or
early adulthood.
disease is a group of inherited disorders that affect metabolism
and are caused by specific genetic mutations. Patients with
Niemann-Pick disease cannot properly metabolize cholesterol and other
lipids. Consequently, excessive amounts of cholesterol accumulate in
the liver and spleen and excessive amounts of other lipids accumulate
in the brain. Symptoms may include dementia, confusion, and problems
with learning and memory. These diseases usually begin in young
school-age children but may also appear during the teen years or
early adulthood.
Batten
disease is a fatal, hereditary disorder of the nervous system
that begins in childhood. Symptoms are linked to a buildup of
substances called lipopigments in the body's tissues. The early
symptoms include personality and behavior changes, slow learning,
clumsiness, or stumbling. Over time, affected children suffer mental
impairment, seizures, and progressive loss of sight and motor skills.
Eventually, children with Batten disease develop dementia and become
blind and bedridden. The disease is often fatal by the late teens or
twenties.
disease is a fatal, hereditary disorder of the nervous system
that begins in childhood. Symptoms are linked to a buildup of
substances called lipopigments in the body's tissues. The early
symptoms include personality and behavior changes, slow learning,
clumsiness, or stumbling. Over time, affected children suffer mental
impairment, seizures, and progressive loss of sight and motor skills.
Eventually, children with Batten disease develop dementia and become
blind and bedridden. The disease is often fatal by the late teens or
twenties.
Lafora
body disease is a rare genetic disease that causes seizures,
rapidly progressive dementia, and movement problems. These problems
usually begin in late childhood or the early teens. Children with
Lafora body disease have microscopic structures called Lafora bodies
in the brain, skin, liver, and muscles. Most affected children die
within 2 to 10 years after the onset of symptoms.
body disease is a rare genetic disease that causes seizures,
rapidly progressive dementia, and movement problems. These problems
usually begin in late childhood or the early teens. Children with
Lafora body disease have microscopic structures called Lafora bodies
in the brain, skin, liver, and muscles. Most affected children die
within 2 to 10 years after the onset of symptoms.
Other
Conditions Causing Dementia
Conditions Causing Dementia
Reactions
to medications
to medications
Medications can sometimes lead to reactions or side effects that
mimic dementia. These dementia-like effects can occur in reaction to just one drug or they can result from drug interactions. They may
have a rapid onset or they may develop slowly over time.
mimic dementia. These dementia-like effects can occur in reaction to just one drug or they can result from drug interactions. They may
have a rapid onset or they may develop slowly over time.
Metabolic
problems and endocrine abnormalities
problems and endocrine abnormalities
Thyroid problems can lead to apathy, depression, or dementia.
Hypoglycemia, a condition in which there is not enough sugar in the
bloodstream, can cause confusion or personality changes. Too little
or too much sodium or calcium can also trigger mental changes. Some
people have an impaired ability to absorb vitamin B12, which creates
a condition called pernicious anemia that can cause personality
changes, irritability, or depression. Tests can determine if any of
these problems are present.
Hypoglycemia, a condition in which there is not enough sugar in the
bloodstream, can cause confusion or personality changes. Too little
or too much sodium or calcium can also trigger mental changes. Some
people have an impaired ability to absorb vitamin B12, which creates
a condition called pernicious anemia that can cause personality
changes, irritability, or depression. Tests can determine if any of
these problems are present.
Nutritional
deficiencies
deficiencies
Deficiencies of thiamine (vitamin B1) frequently result from chronic
alcoholism and can seriously impair mental abilities, in particular
memories of recent events. Severe deficiency of vitamin B6 can cause
a neurological illness called pellagra that may include dementia.
Deficiencies of vitamin B12 also have been linked to dementia in some
cases. Dehydration can also cause mental impairment that can resemble
dementia.
alcoholism and can seriously impair mental abilities, in particular
memories of recent events. Severe deficiency of vitamin B6 can cause
a neurological illness called pellagra that may include dementia.
Deficiencies of vitamin B12 also have been linked to dementia in some
cases. Dehydration can also cause mental impairment that can resemble
dementia.
Infections
Many infections can cause neurological symptoms, including confusion
or delirium, due to fever or other side effects of the body's fight
to overcome the infection. Meningitis and encephalitis, which are
infections of the brain or the membrane that covers it, can cause
confusion, sudden severe dementia, withdrawal from social
interaction, impaired judgment, or memory loss. Untreated syphilis
also can damage the nervous system and cause dementia. In rare cases,
Lyme disease can cause memory or thinking difficulties. People in the
advanced stages of AIDS also may develop a form of dementia (see
HIV-associated dementia). People with compromised immune systems,
such as those with leukemia and AIDS, may also develop an infection
called progressive multifocal leukoencephalopathy (PML). PML is
caused by a common human polyomavirus, JC virus, and leads to damage
or destruction of the myelin sheath that covers nerve cells. PML can
lead to confusion, difficulty with thinking or speaking, and other
mental problems.
or delirium, due to fever or other side effects of the body's fight
to overcome the infection. Meningitis and encephalitis, which are
infections of the brain or the membrane that covers it, can cause
confusion, sudden severe dementia, withdrawal from social
interaction, impaired judgment, or memory loss. Untreated syphilis
also can damage the nervous system and cause dementia. In rare cases,
Lyme disease can cause memory or thinking difficulties. People in the
advanced stages of AIDS also may develop a form of dementia (see
HIV-associated dementia). People with compromised immune systems,
such as those with leukemia and AIDS, may also develop an infection
called progressive multifocal leukoencephalopathy (PML). PML is
caused by a common human polyomavirus, JC virus, and leads to damage
or destruction of the myelin sheath that covers nerve cells. PML can
lead to confusion, difficulty with thinking or speaking, and other
mental problems.
Subdural
hematomas
hematomas
Subdural hematomas, or bleeding between the brain's surface and its
outer covering (the dura), can cause dementia-like symptoms and
changes in mental function.
outer covering (the dura), can cause dementia-like symptoms and
changes in mental function.
Poisoning
Exposure to lead, other heavy metals, or other poisonous substances
can lead to symptoms of dementia. These symptoms may or may not
resolve after treatment, depending on how badly the brain is damaged.
People who have abused substances such as alcohol and recreational
drugs sometimes display signs of dementia even after the substance
abuse has ended. This condition is known as substance-induced
persisting dementia.
Exposure to lead, other heavy metals, or other poisonous substances
can lead to symptoms of dementia. These symptoms may or may not
resolve after treatment, depending on how badly the brain is damaged.
People who have abused substances such as alcohol and recreational
drugs sometimes display signs of dementia even after the substance
abuse has ended. This condition is known as substance-induced
persisting dementia.
Brain
tumors
tumors
In rare cases, people with brain tumors may develop dementia because
of damage to their brains. Symptoms may include changes in
personality, psychotic episodes, or problems with speech, language,
thinking, and memory.
of damage to their brains. Symptoms may include changes in
personality, psychotic episodes, or problems with speech, language,
thinking, and memory.
Anoxia
Anoxia and a related term, hypoxia, are often used interchangeably to
describe a state in which there is a diminished supply of oxygen to
an organ's tissues. Anoxia may be caused by many different problems,
including heart attack, heart surgery, severe asthma, smoke or carbon
monoxide inhalation, high-altitude exposure, strangulation, or an
overdose of anesthesia. In severe cases of anoxia the patient may be
in a stupor or a coma for periods ranging from hours to days, weeks,
or months. Recovery depends on the severity of the oxygen
deprivation. As recovery proceeds, a variety of psychological and
neurological abnormalities, such as dementia or psychosis, may occur.
The person also may experience confusion, personality changes,
hallucinations, or memory loss.
Anoxia and a related term, hypoxia, are often used interchangeably to
describe a state in which there is a diminished supply of oxygen to
an organ's tissues. Anoxia may be caused by many different problems,
including heart attack, heart surgery, severe asthma, smoke or carbon
monoxide inhalation, high-altitude exposure, strangulation, or an
overdose of anesthesia. In severe cases of anoxia the patient may be
in a stupor or a coma for periods ranging from hours to days, weeks,
or months. Recovery depends on the severity of the oxygen
deprivation. As recovery proceeds, a variety of psychological and
neurological abnormalities, such as dementia or psychosis, may occur.
The person also may experience confusion, personality changes,
hallucinations, or memory loss.
Heart
and lung problems
and lung problems
The brain requires a high level of oxygen in order to carry out its
normal functions. Therefore, problems such as chronic lung disease or
heart problems that prevent the brain from receiving adequate oxygen
can starve brain cells and lead to the symptoms of dementia.
normal functions. Therefore, problems such as chronic lung disease or
heart problems that prevent the brain from receiving adequate oxygen
can starve brain cells and lead to the symptoms of dementia.
Conditions
That Are Not Dementia
That Are Not Dementia
Age-related
cognitive decline
cognitive decline
As
people age, they usually experience slower information processing and
mild memory impairment. In addition, their brains frequently decrease
in volume and some nerve cells, or neurons, are lost. These changes,
called age-related cognitive decline, are normal and are not
considered signs of dementia.
people age, they usually experience slower information processing and
mild memory impairment. In addition, their brains frequently decrease
in volume and some nerve cells, or neurons, are lost. These changes,
called age-related cognitive decline, are normal and are not
considered signs of dementia.
Mild
cognitive impairment
cognitive impairment
Some people develop cognitive and memory problems that are not
severe enough to be diagnosed as dementia but are more pronounced
than the cognitive changes associated with normal aging. This
condition is called mild cognitive impairment. Although many patients
with this condition later develop dementia, some do not. Many
researchers are studying mild cognitive impairment to find ways to
treat it or prevent it from progressing to dementia.
severe enough to be diagnosed as dementia but are more pronounced
than the cognitive changes associated with normal aging. This
condition is called mild cognitive impairment. Although many patients
with this condition later develop dementia, some do not. Many
researchers are studying mild cognitive impairment to find ways to
treat it or prevent it from progressing to dementia.
Depression
People with depression are frequently passive or unresponsive, and
they may appear slow, confused, or forgetful. Other emotional
problems can also cause symptoms that sometimes mimic dementia.
People with depression are frequently passive or unresponsive, and
they may appear slow, confused, or forgetful. Other emotional
problems can also cause symptoms that sometimes mimic dementia.
Delirium
Delirium is characterized by confusion and rapidly altering mental
states. The person may also be disoriented, drowsy, or incoherent,
and may exhibit personality changes. Delirium is usually caused by a
treatable physical or psychiatric illness, such as poisoning or
infections. Patients with delirium often, though not always, make a
full recovery after their underlying illness is treated.
states. The person may also be disoriented, drowsy, or incoherent,
and may exhibit personality changes. Delirium is usually caused by a
treatable physical or psychiatric illness, such as poisoning or
infections. Patients with delirium often, though not always, make a
full recovery after their underlying illness is treated.
Causes
Of Dementia
Of Dementia
All forms of dementia result from the death of nerve cells and/or the
loss of communication among these cells. The human brain is a very
complex and intricate machine and many factors can interfere with its
functioning. Researchers have uncovered many of these factors, but
they have not yet been able to fit these puzzle pieces together in
order to form a complete picture of how dementias develop.
loss of communication among these cells. The human brain is a very
complex and intricate machine and many factors can interfere with its
functioning. Researchers have uncovered many of these factors, but
they have not yet been able to fit these puzzle pieces together in
order to form a complete picture of how dementias develop.
Many types of dementia, including AD, Lewy body dementia, Parkinson's
dementia, and Pick's disease, are characterized by abnormal
structures called inclusions in the brain. Because these inclusions,
which contain abnormal proteins, are so common in people with
dementia, researchers suspect that they play a role in the
development of symptoms. However, that role is unknown, and in some
cases the inclusions may simply be a side effect of the disease
process that leads to the dementia.
dementia, and Pick's disease, are characterized by abnormal
structures called inclusions in the brain. Because these inclusions,
which contain abnormal proteins, are so common in people with
dementia, researchers suspect that they play a role in the
development of symptoms. However, that role is unknown, and in some
cases the inclusions may simply be a side effect of the disease
process that leads to the dementia.
Genes clearly play a role in the development of some kinds of
dementia. However, in AD and many other disorders, the dementia
usually cannot be tied to a single abnormal gene. Instead, these
forms of dementia appear to result from a complex interaction of
genes, lifestyle factors, and other environmental influences.
dementia. However, in AD and many other disorders, the dementia
usually cannot be tied to a single abnormal gene. Instead, these
forms of dementia appear to result from a complex interaction of
genes, lifestyle factors, and other environmental influences.
Researchers have identified several genes that influence
susceptibility to AD. Mutations in three of the known genes for AD -
genes that control the production of proteins such as amyloid
precursor protein (APP), presenilin 1, and presenilin 2 - are linked
to early-onset forms of the disease.
susceptibility to AD. Mutations in three of the known genes for AD -
genes that control the production of proteins such as amyloid
precursor protein (APP), presenilin 1, and presenilin 2 - are linked
to early-onset forms of the disease.
Variations in another gene, called apolipoprotein E (apoE), have been
linked to an increased risk of late-onset AD. The apoE gene does not
cause the disease by itself, but one version of the gene, called apoE
epsilon4 (apoE E4), appears to increase the risk of AD. People with
two copies of the apoE E4 gene have about ten times the risk of
developing AD compared to people without apoE E4. This gene variant
seems to encourage amyloid deposition in the brain. One study also
found that this gene is associated with shorter survival in men with
AD. In contrast, another version of the apoE gene, called apoE E2,
appears to protect against AD.
linked to an increased risk of late-onset AD. The apoE gene does not
cause the disease by itself, but one version of the gene, called apoE
epsilon4 (apoE E4), appears to increase the risk of AD. People with
two copies of the apoE E4 gene have about ten times the risk of
developing AD compared to people without apoE E4. This gene variant
seems to encourage amyloid deposition in the brain. One study also
found that this gene is associated with shorter survival in men with
AD. In contrast, another version of the apoE gene, called apoE E2,
appears to protect against AD.
Studies have suggested that mutations in another gene, called CYP46,
may contribute to an increased risk of developing late-onset sporadic
AD. This gene normally produces a protein that helps the brain
metabolize cholesterol.
may contribute to an increased risk of developing late-onset sporadic
AD. This gene normally produces a protein that helps the brain
metabolize cholesterol.
Scientists are trying to determine how beta amyloid influences the
development of AD. A number of studies indicate that the buildup of
this protein initiates a complex chain of events that culminates in
dementia. One study found that beta amyloid buildup in the brain
triggers cells called microglia, which act like janitors that mop up
potentially harmful substances in the brain, to release a potent
neurotoxin called peroxynitrite. This may contribute to nerve cell
death in AD. Another study found that beta amyloid causes a protein
called p35 to be split into two proteins. One of the resulting
proteins triggers changes in the tau protein that lead to formation
of neurofibrillary tangles. A third study found that beta amyloid
activates cell-death enzymes called caspases that alter the tau
protein in a way that causes it to form tangles. Researchers believe
these tangles may contribute to the neuron death in AD.
development of AD. A number of studies indicate that the buildup of
this protein initiates a complex chain of events that culminates in
dementia. One study found that beta amyloid buildup in the brain
triggers cells called microglia, which act like janitors that mop up
potentially harmful substances in the brain, to release a potent
neurotoxin called peroxynitrite. This may contribute to nerve cell
death in AD. Another study found that beta amyloid causes a protein
called p35 to be split into two proteins. One of the resulting
proteins triggers changes in the tau protein that lead to formation
of neurofibrillary tangles. A third study found that beta amyloid
activates cell-death enzymes called caspases that alter the tau
protein in a way that causes it to form tangles. Researchers believe
these tangles may contribute to the neuron death in AD.
Vascular dementia can be caused by cerebrovascular disease or any
other condition that prevents normal blood flow to the brain. Without
a normal supply of blood, brain cells cannot obtain the oxygen they
need to work correctly, and they often become so deprived that they
die.
other condition that prevents normal blood flow to the brain. Without
a normal supply of blood, brain cells cannot obtain the oxygen they
need to work correctly, and they often become so deprived that they
die.
The causes of other types of dementias vary. Some, such as CJD and
GSS, have been tied to abnormal forms of specific proteins. Others,
including Huntington's disease and FTDP-17, have been linked to
defects in a single gene. Post-traumatic dementia is directly related
to brain cell death after injury. HIV-associated dementia is clearly
tied to infection by the HIV virus, although the exact way the virus
causes damage is not yet certain. For other dementias, such as
corticobasal degeneration and most types of frontotemporal dementia,
the underlying causes have not yet been identified.
GSS, have been tied to abnormal forms of specific proteins. Others,
including Huntington's disease and FTDP-17, have been linked to
defects in a single gene. Post-traumatic dementia is directly related
to brain cell death after injury. HIV-associated dementia is clearly
tied to infection by the HIV virus, although the exact way the virus
causes damage is not yet certain. For other dementias, such as
corticobasal degeneration and most types of frontotemporal dementia,
the underlying causes have not yet been identified.
Risk
Factors for Dementia
Factors for Dementia
Age. The risk
of AD, vascular dementia, and several other dementias goes up
significantly with advancing age.
Genetics/family
history. As described in the section "What Causes
Dementia?" researchers have discovered a number of genes that
increase the risk of developing AD. Although people with a family
history of AD are generally considered to be at heightened risk of
developing the disease themselves, many people with a family history
never develop the disease, and many without a family history of the
disease do get it. In most cases, it is still impossible to predict
a specific person's risk of the disorder based on family history
alone. Some families with CJD, GSS, or fatal familial insomnia have
mutations in the prion protein gene, although these disorders can
also occur in people without the gene mutation. Individuals with
these mutations are at significantly higher risk of developing these
forms of dementia. Abnormal genes are also clearly implicated as
risk factors in Huntington's disease, FTDP-17, and several other
kinds of dementia. These dementias are described in the section
"What are the different kinds of dementia?"
Smoking and
alcohol use. Several recent studies have found that smoking
significantly increases the risk of mental decline and dementia.
People who smoke have a higher risk of atherosclerosis and other
types of vascular disease, which may be the underlying causes for
the increased dementia risk. Studies also have found that drinking
large amounts of alcohol appears to increase the risk of dementia.
However, other studies have suggested that people who drink
moderately have a lower risk of dementia than either those who drink
heavily or those who completely abstain from drinking.
Atherosclerosis.
Atherosclerosis is the buildup of plaque - deposits of fatty
substances, cholesterol, and other matter - in the inner lining of
an artery. Atherosclerosis is a significant risk factor for vascular
dementia, because it interferes with the delivery of blood to the
brain and can lead to stroke. Studies have also found a possible
link between atherosclerosis and AD.
Cholesterol.
High levels of low-density lipoprotein (LDL), the so-called bad form
of cholesterol, appear to significantly increase a person's risk of
developing vascular dementia. Some research has also linked high
cholesterol to an increased risk of AD.
Plasma
homocysteine. Research has shown that a higher-than-average
blood level of homocysteine - a type of amino acid - is a strong
risk factor for the development of AD and vascular dementia.
Diabetes.
Diabetes is a risk factor for both AD and vascular dementia. It is
also a known risk factor for atherosclerosis and stroke, both of
which contribute to vascular dementia.
Mild cognitive
impairment. While not all people with mild cognitive impairment
develop dementia, people with this condition do have a significantly
increased risk of dementia compared to the rest of the population.
One study found that approximately 40 percent of people over age 65
who were diagnosed with mild cognitive impairment developed dementia
within 3 years.
Down syndrome.
Studies have found that most people with Down syndrome develop
characteristic AD plaques and neurofibrillary tangles by the time
they reach middle age. Many, but not all, of these individuals also
develop symptoms of dementia.
Diagnosis
Doctors employ a number of strategies to diagnose dementia. It is
important that they rule out any treatable conditions, such as
depression, normal pressure hydrocephalus, or vitamin B12 deficiency,
which can cause similar symptoms.
important that they rule out any treatable conditions, such as
depression, normal pressure hydrocephalus, or vitamin B12 deficiency,
which can cause similar symptoms.
Early, accurate diagnosis of dementia is important for patients and
their families because it allows early treatment of symptoms. For
people with AD or other progressive dementias, early diagnosis may
allow them to plan for the future while they can still help to make
decisions. These people also may benefit from drug treatment.
their families because it allows early treatment of symptoms. For
people with AD or other progressive dementias, early diagnosis may
allow them to plan for the future while they can still help to make
decisions. These people also may benefit from drug treatment.
The "gold standard" for diagnosing dementia, autopsy, does
not help the patient or caregivers. Therefore, doctors have devised a
number of techniques to help identify dementia with reasonable
accuracy while the patient is still alive.
not help the patient or caregivers. Therefore, doctors have devised a
number of techniques to help identify dementia with reasonable
accuracy while the patient is still alive.
Patient history:
Doctors often begin their examination of a patient suspected of
having dementia by asking questions about the patient's history. For
example, they may ask how and when symptoms developed and about the
patient's overall medical condition. They also may try to evaluate
the patient's emotional state, although patients with dementia often
may be unaware of or in denial about how their disease is affecting
them. Family members also may deny the existence of the disease
because they do not want to accept the diagnosis and because, at
least in the beginning, AD and other forms of dementia can resemble
normal aging. Therefore additional steps are necessary to confirm or
rule out a diagnosis of dementia.
Physical
examination: A physical examination can help rule out treatable
causes of dementia and identify signs of stroke or other disorders
that can contribute to dementia. It can also identify signs of other
illnesses, such as heart disease or kidney failure, that can overlap
with dementia. If a patient is taking medications that may be
causing or contributing to his or her symptoms, the doctor may
suggest stopping or replacing some medications to see if the
symptoms go away.
Neurological
evaluations: Doctors will perform a neurological examination,
looking at balance, sensory function, reflexes, and other functions,
to identify signs of conditions - for example movement disorders or
stroke - that may affect the patient's diagnosis or are treatable
with drugs.
Cognitive and
neuropsychological tests: Doctors use tests that measure memory,
language skills, math skills, and other abilities related to mental
functioning to help them diagnose a patient's condition accurately.
For example, people with AD often show changes in so-called
executive functions (such as problem-solving), memory, and the
ability to perform once-automatic tasks.
Doctors often use a
test called the Mini-Mental State Examination (MMSE) to
assess cognitive skills in people with suspected dementia. This test
examines orientation, memory, and attention, as well as the ability
to name objects, follow verbal and written commands, write a
sentence spontaneously, and copy a complex shape. Doctors also use a
variety of other tests and rating scales to identify specific types
of cognitive problems and abilities.
Brain scans:
Doctors may use brain scans to identify strokes, tumors, or other
problems that can cause dementia. Also, cortical atrophy
-degeneration of the brain's cortex (outer layer) - is common in
many forms of dementia and may be visible on a brain scan. The
brain's cortex normally appears very wrinkled, with ridges of tissue
(called gyri) separated by "valleys" called sulci. In
individuals with cortical atrophy, the progressive loss of neurons
causes the ridges to become thinner and the sulci to grow wider. As
brain cells die, the ventricles (or fluid-filled cavities in the
middle of the brain) expand to fill the available space, becoming
much larger than normal. Brain scans also can identify changes in
the brain's structure and function that suggest AD. The most common
types of brain scans are computed tomographic (CT) scans and
magnetic resonance imaging (MRI). Doctors frequently request a CT
scan of the brain when they are examining a patient with suspected
dementia. These scans, which use X-rays to detect brain structures,
can show evidence of brain atrophy, strokes and transient ischemic
attacks (TIAs), changes to the blood vessels, and other problems
such as hydrocephalus and subdural hematomas. MRI scans use magnetic
fields and focused radio waves to detect hydrogen atoms in tissues
within the body. They can detect the same problems as CT scans but
they are better for identifying certain conditions, such as brain
atrophy and damage from small TIAs.
Doctors also may use
electroencephalograms (EEGs) in people with suspected
dementia. In an EEG, electrodes are placed on the scalp over several
parts of the brain in order to detect and record patterns of
electrical activity and check for abnormalities. This electrical
activity can indicate cognitive dysfunction in part or all of the
brain. Many patients with moderately severe to severe AD have
abnormal EEGs. An EEG may also be used to detect seizures, which
occur in about 10 percent of AD patients as well as in many other
disorders. EEGs also can help diagnose CJD.
Several other types
of brain scans allow researchers to watch the brain as it functions.
These scans, called functional brain imaging, are not often used as
diagnostic tools, but they are important in research and they may
ultimately help identify people with dementia earlier than is
currently possible. Functional brain scans include functional MRI
(fMRI), single photon-emission computed tomography (SPECT), positron
emission tomography (PET), and magnetoencephalography (MEG). fMRI
uses radio waves and a strong magnetic field to measure the
metabolic changes that take place in active parts of the brain.
SPECT shows the distribution of blood in the brain, which generally
increases with brain activity. PET scans can detect changes in
glucose metabolism, oxygen metabolism, and blood flow, all of which
can reveal abnormalities of brain function. MEG shows the
electromagnetic fields produced by the brain's neuronal activity.
Laboratory
tests
tests
Doctors may use a variety of laboratory tests to help diagnose
dementia and/or rule out other conditions, such as kidney failure,
that can contribute to symptoms. A partial list of these tests
includes a complete blood count, blood glucose test, urinalysis, drug
and alcohol tests (toxicology screen), cerebrospinal fluid analysis
(to rule out specific infections that can affect the brain), and
analysis of thyroid and thyroid-stimulating hormone levels. A doctor
will order only the tests that he or she feels are necessary and/or
likely to improve the accuracy of a diagnosis.
dementia and/or rule out other conditions, such as kidney failure,
that can contribute to symptoms. A partial list of these tests
includes a complete blood count, blood glucose test, urinalysis, drug
and alcohol tests (toxicology screen), cerebrospinal fluid analysis
(to rule out specific infections that can affect the brain), and
analysis of thyroid and thyroid-stimulating hormone levels. A doctor
will order only the tests that he or she feels are necessary and/or
likely to improve the accuracy of a diagnosis.
Psychiatric
evaluation
evaluation
A psychiatric evaluation may be obtained to determine if depression
or another psychiatric disorder may be causing or contributing to a
person's symptoms.
or another psychiatric disorder may be causing or contributing to a
person's symptoms.
Presymptomatic
testing
testing
Testing people before symptoms begin to determine if they will
develop dementia is not possible in most cases. However, in disorders
such as Huntington's where a known gene defect is clearly linked to
the risk of the disease, a genetic test can help identify people who
are likely to develop the disease. Since this type of genetic
information can be devastating, people should carefully consider
whether they want to undergo such testing.
develop dementia is not possible in most cases. However, in disorders
such as Huntington's where a known gene defect is clearly linked to
the risk of the disease, a genetic test can help identify people who
are likely to develop the disease. Since this type of genetic
information can be devastating, people should carefully consider
whether they want to undergo such testing.
Researchers are examining whether a series of simple cognitive tests,
such as matching words with pictures, can predict who will develop
dementia. One study suggested that a combination of a verbal learning
test and an odor-identification test can help identify AD before
symptoms become obvious. Other studies are looking at whether memory
tests and brain scans can be useful indicators of future dementia.
such as matching words with pictures, can predict who will develop
dementia. One study suggested that a combination of a verbal learning
test and an odor-identification test can help identify AD before
symptoms become obvious. Other studies are looking at whether memory
tests and brain scans can be useful indicators of future dementia.
Prevention
Of Dementia
Of Dementia
Possible preventive actions include:
Lowering
homocysteine: In one study, elevated blood levels of the amino
acid homocysteine were associated with a 2.9 times greater risk of
AD and a 4.9 times greater risk of vascular dementia. A preliminary
study has shown that high doses of three B vitamins that help lower
homocysteine levels - folic acid, B12, and B6 - appear to slow the
progression of AD. Researchers are conducting a multi-center
clinical trial to test this effect in a larger group of patients.
Lowering
cholesterol levels: Research has suggested that people with high
cholesterol levels have an increased risk of developing AD.
Cholesterol is involved in formation of amyloid plaques in the
brain. Mutations in a gene called CYP46 and the apoE E4 gene
variant, both of which have been linked to an increased risk of AD,
are also involved in cholesterol metabolism. Several studies have
also found that the use of drugs called statins, which lower
cholesterol levels, is associated with a lower likelihood of
cognitive impairment.
Lowering
blood pressure: Several studies have shown that antihypertensive
medicine reduces the odds of cognitive impairment in elderly people
with high blood pressure. One large European study found a 55
percent lower risk of dementia in people over 60 who received drug
treatment for hypertension. These people had a reduced risk of both
AD and vascular dementia.
Exercise:
Regular exercise stimulates production of chemicals called growth
factors that help neurons survive and adapt to new situations. These
gains may help to delay the onset of dementia symptoms. Exercise
also may reduce the risk of brain damage from atherosclerosis.
Education:
Researchers have found evidence that formal education may help
protect people against the effects of AD. In one study, researchers
found that people with more years of formal education had relatively
less mental decline than people with less schooling, regardless of
the number of amyloid plaques and neurofibrillary tangles each
person had in his or her brain. The researchers think education may
cause the brain to develop robust nerve cell networks that can help
compensate for the cell damage caused by AD.
Controlling
inflammation: Many studies have suggested that inflammation may
contribute to AD. Moreover, autopsies of people who died with AD
have shown widespread inflammation in the brain that appeared to be
caused by the accumulation of beta amyloid. Another study found that
men with high levels of C-reactive protein, a general marker of
inflammation, had a significantly increased risk of AD and other
kinds of dementia.
Medicinal
Management
Management
Anacardium
Fixed
ideas.
Hallucinations;
thinks he is possessed of two persons or wills.
Anxiety
when walking, as if pursued.
Profound
melancholy and hypochondriasis, with tendency to use violent
language.
Brain-fag.
Impaired memory.
Absent
mindedness.
Very
easily offended.
Malicious; seems bent on wickedness.
Lack of confidence in himself or others.
Suspicious.
Clairaudient,
hears voices far away or of the dead.
Senile
dementia.
Absence
of all moral restraint.
Total
loss of memory, mental dullness, and confusion.
Incomplete
paralysis paralysis of involuntary muscles.
Disposed
to be malicious.
Seems
bent on wickedness.
Irresistible
desire to curse and swear.
Strange
temper-laugh at serious matters and is serious over laughable
things.
Think
herself a demon, curses and swears.
Sensation
of a loop or band around a part.
Headache
relieved entirely when eating.
Worse
during motion and work.
Belladonna
Patient lives in a
world of his own, engrossed by spectres and visions and oblivious
to surrounding realities.
While the retina
is insensible to actual objects, a host of visual hallucinations
throng about him and come to him from within.
He is acutely
alive and crazed by a flood of subjective visual impressions and
fantastic illusions.
Hallucinations-sees
monsters, hideous faces.
Delirium;
frightful images; furious; rages, bites, strikes; desire to escape.
Loss of
consciousness.
Disinclined to
talk.
Perversity, with
tears.
Acuteness of all
senses.
Changeableness.
Vertigo, with
falling to left side or backwards.
Sensitive to least
contact.
Agaricus
Sings, talks, but
does not answer.
Loquacity.
Aversion to work.
Indifference.
Fearlessness.
Delirium
characterized by singing, shouting, and muttering; rhymes and
prophesies. Begins with paroxysm of yawning.
The provings
bring out four phases of cerebral excitement.
1. Slight stimulation -- shown by increased cheerfulness, courage,
loquacity, exalted fancy.
2. More decided intoxication great mental excitement and incoherent
talking, immoderate gaiety alternates with melancholy. Perception of
relative size of objects is lost, takes long steps and jumps over
small objects as if they were trunks of trees -- a small hole appears
as a frightful chasm, a spoonful of water an immense lake. Physical
strength is increased, can lift heavy loads. With it much twitching.
3.
Third stage- produces a condition of furious or raging delirium,
screaming, raving, wants to injure himself, etc.
Third stage- produces a condition of furious or raging delirium,
screaming, raving, wants to injure himself, etc.
4. Fourth stage -- mental depression, languor, indifference,
confusion, disinclination to work, etc. We do not get the active
cerebral congestion of Belladonna, but a general nervous
excitement such as is found in delirium tremens, delirium of
fevers, etc.
Paralysis of lower
limbs, with spasmodic condition of arms.
Numbness of legs
on crossing them.
Hyoscymus
Disturbs the
nervous system profoundly.
It is as if some
diabolical force took possession of the brain and prevented its
functions.
It causes a
perfect picture of mania of a quarrelsome and obscene character.
Inclined to be
unseemly and immodest in acts, gestures and expressions.
Very talkative,
and persists in stripping herself, or uncovering genitals.
Is jealous, afraid
of being poisoned, etc.
Its symptoms also
point to weakness and nervous agitation; hence typhoid and other
infections with coma vigil.
Tremulous weakness
and twitching of tendons.
Subsultus
tendinum.
Muscular
twitchings, spasmodic affections, generally with delirium.
Non-inflammatory
cerebral activity.
Very suspicious.
Talkative,
obscene, lascivious mania, uncovers body; jealous, foolish.
Great hilarity;
inclined to laugh at everything.
Delirium, with
attempt to run away.
Low, muttering
speech; constant carphologia, deep stupor.
Feels light and
confused.
Vertigo as if
intoxicated.
Brain feels
loose, fluctuating.
Inflammation of
brain, with unconsciousness; head is shaken to and fro.
Eyes open, but
does not pay attention; downcast and dull, fixed.
Epileptic attacks
ending in deep sleep.
Phosphoric
Acid
Mental debility
first; later physical.
A congenial soil
for the action of phosphoric acid is found in young people who grow
rapidly, and who are overtaxed, mentally or physically.
Whenever the
system has been exposed to the ravages of acute disease, excesses,
grief, loss of vital fluids, we obtain conditions calling
for it.
Listless.
Impaired memory.
Apathetic,
indifferent.
Cannot collect his
thoughts or find the right word.
Difficult
comprehension.
Effects of grief
and mental shock.
Delirium, with
great stupefaction.
Settled despair.
Phosphorus
Great lowness of
spirits. Easily vexed.
Fearfulness, as if
something were creeping out of every corner.
Clairvoyant state.
Great tendency to
start. Over-sensitive to external impressions.
Loss of memory.
Paralysis of the
insane.
Ecstasy.
Dread of death
when alone.
Brain feels tired.
Insanity, with an
exaggerated idea of one's own importance.
Excitable,
produces heat all over.
Restless, fidgety.
Hypo-sensitive,
indifferent.
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